• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/16

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

16 Cards in this Set

  • Front
  • Back
toxicities of all TNF alpha inhibitors used in treatment of RA...
infection, lymphoma, hepatotoxicity, hematological effects HS reactions, CVS toxicity...
tnf alpha inhibs and biological agents give to RA patient when...
other DMARDs as mono therapy have failed
given by IV infusion in combination with oral methotrexate at 0, 2, 6 weeks, and then once every 8

HS infusion reaction may occur - can give acetaminophen or diphenhydramine (h1block)

Use for RA, together with methotrex
-also for ankylosing spondylitis or crohn's

hman/mouse chimeric IgG1 monoclonal ab, against TNF alpha.

binds both bound and soluble tnf-a
higher affinity than other biological drugs that are soluble receptors
inflixamab
MOA
binds to soluble and membrane bound TNF alpha

SC injection every 14 days. self administered injection pen.

use for RA, ankylosing spondylitis, crown's

MOA
-blocks TNFa
reduces levels of C reactive protein
reduces ESR
reduces serum IL 6
reduces matrix metallo proteinases MMP 1 and 3 (secreted by fibroblast in response to cytokines. degrade the matrix)

half life of 2 weeks is increased in patines also taking methotrexate

BLACK BOX
TB
invasive funal infections
opportunistics

AEs
exacerbates chronic CHF
serious infections
Lupus like syndrome

its a fully humanized monoclonal IgG1 antibody
adalimumab
a soluble tnf a RECEPTOR

binds soluble and membrane bound tnf a

use for moderate to severe RA

AEs
injection site reaction
autoantibody formation
HS reactions
infections
increased risk of cancer

Contrain:
documented HS
sepsis
concurrent live vaccinations


SC injection once a week
etanercept
recombinant for of human IL-1 receptor antagonist

extracted from e. coli

short half life give daily. binds to IL 1 receptor and decreases production of inflammatory cytokines

use for RA

AEs
headache
gastro
injection site reaction is strong

Serious AEs
infections**
decrease white cell
antibody formation against the drug itself
anakinra
these DMARDS are...
-slow to act (months)
no direct analgesic actions
slow course of disease
given to NSAID non responders and non compliant its, and those with serious GIT problems with NSAIDS and steroids
-to patients whose joints are deteriorating rapidly
-for juvenile RA
D-penicillamine
chloroquine and hydroxy-
sulfonamide plus salicylate=sulfasalazine
symptoms alleviated: reductes # of T lymphs, IL 1, RF, and inhibits macros

MOA UNKNOWN.

use if other drugs have failed in RA patients

major use is Wilson's disease (it chelates copper)

take orally, plasma concentrations peak 1-2 hrs, but doesn't become clinically effective for months

***platelets, CBC and urinalysis before and therapy and then every 2-4 weeks. see AEs

AEs
cutaneous lesions
blood dyscrasias - BM SUPPRESSION
proteinuiria (when RA pts develop this, switch out of DMARD class altogether, don't substitute new DMARD)
HS reactions (highly contrained in goodpastures syndrome)
-M.Gravis can be induced by long term use

teratogenic
penicillamine
second line RA drugs

MOA
suppresses responsiveness of T lymphs to mitogens
-decreassed leukocyte chemotaxid
-stabalizes lysosomal membranes (where the drug concentrates)
-inhibits DNA and RNA synth
-traps free radicals, reducing oxidative reactions which may be ass'd with deteriorating bone

take after meals. 4-12 weeks before discernible improvements seen

AEs are mild
-dermatitis
myopathy
reversible corneal opacity
GI irritation
nightmares
*irreversible retinal degernation - dose and freq. related. opthalmic exam every six months. symptoms: night blindness, blurred vision, missing or blanched out areas of central or peripheral fields, light flashes/streaks/photophobia
hydroxychloroquine

chloroquine
prodrug used for ulcerative colitis, RA, IBD, and RA

oral, then metabolized by gut bacteria to 5-aminosalicylic acid aka mesalamine aka sulfapyridine.

inhibition of cyclooxygenases in the gut, diminished PG production

slow acetylators have increased incidence of AEs

NVD, anorrexia, rash and serum sickness.
*leukopenia, thrombocytopenia, allopecia, elevated liver enzymes: occur within first 3-6 months then abate. reverse when treatment stops.
sulfasalazine
most commonly prescribed DMARD

used in combo with anti-TNF

reduces signs and symptoms and slows progression

AEs
NVD
leucopenia
lung issues...
HS reaction (can develop anytime during use)
hepatotoxicity (slow, with accumulative dosing. long term -> hepatic fibrosis)
methotrexate
use for moderate to severe RA and psoriatic arthritis

inhitbits pyrimidine synthesis
inhibits T and B roliferations
leflunomide
inhibits the reabsorption of urate FROM TEH LUMEN at the PT.

oral

bound to albumin 90%
-free drug passes into the glomerular filtrate, but more is actively secreted into the PT, where it may diffuse back because of its high lipid solubility

(if given in sub tx doses, actually inhibit the secretion of the compound they are meant to increase excretion of)
probenicid
the 'other' uricosuric

inhibits reabsorption in PT
sulphinpyrazone
for long term tx of gout. not acute.

prevents production of uric acid

metabolized by key enzyme, and its metabolite inhibits that enzyme, competitively, reducing production of uric acid

INTERACTIONS
1 - drug increases the half life of probenicid... and probenicid increases the clearance of the drug's active metabolite. thus increase dose of allopurinol
2 - active metabolite decreases metabolism of azathiaprine and mercaptopurine. decrease doses of both.
3 - if given with theophylline (a xanthine), leads to an increased accumulation of 1-methyl xanthine, the active metabolite of theophylline (?)
allopurinol
unique antiinflammatory, effective only against acute gouty arthritis

reduces pain and swelling <12 hrs

MOA
inhibits cells division: binds to tubulin, preventing microtubules
inhibits leukocyte migration into joints
blocks lipoxygenase enzymes, thus blocking in inflammatory leukotrienes

dramatic pain relief

oral/IV

interhepatic reciurculation
drug secretion into bile mediated by MDR protein pump
drugs that inhibit MDR... lower dose of ""

side effects limit chronic usage:
serious GI toxicity
myelosuppressive
agranulocytosis
aplastic anemia
myopathy
alopecia
colchicine